Ask about this productRelated genes to: DFF45 antibody
- Gene:
- DFFA NIH gene
- Name:
- DNA fragmentation factor subunit alpha
- Previous symbol:
- -
- Synonyms:
- DFF-45, DFF45, ICAD, DFF1
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-27
- Date modifiied:
- 2016-10-05
Related products to: DFF45 antibody
Related articles to: DFF45 antibody
- Breast cancer continues to be a major contributor to cancer-associated deaths among the female population globally. This study aims to investigate the functional role, underlying mechanisms, and clinical relevance of Cell death-inducing DFFA-like effector C (CIDEC) in breast cancer pathogenesis. - Source: PubMed
Publication date: 2026/04/20
Jin XuchuLiu YuZheng XinyuHe Yangke - In colorectal carcinoma (CRC), 5-fluorouracil (5-FU) remains the cornerstone of adjuvant systemic therapy, with folic acid (FA) serving as an essential adjunct. Expression of genes related to the metabolism and action of 5-FU and FA can be influenced by patient- and tumor-specific biological factors. In this study, we explore differential gene expression profiles of 180 genes representing 14 different gene sets associated with different 5-FU and FA metabolism processes, at both gene and pathway levels across clinical and molecular subgroups. In 71 patients with CRC, paired tumors and normal colonic tissues were analyzed. In CRC tissue, several gene sets (including Cell Cycle Checkpoint, Oxidative Stress Response, and Signaling Pathway, etc.) were upregulated, while three gene sets (Apoptotic, Tumor Suppressor, and Endoplasmic Reticulum Stress) were downregulated. Kirsten rat sarcoma virus (), tumor protein p53 (), and microsatellite instability (MSI) status impacted gene expression across molecular subgroups. At the individual gene level, among cell cycle genes, the BUB3 mitotic checkpoint protein () was upregulated in MSI tumors compared to MSS, whereas SMAD family member 4 () was downregulated in MSS tumors compared to MSI. DNA fragmentation factor alpha () was downregulated in MSI and upregulated in MSS. Notably, thymidylate synthetase () was more upregulated in MSI tumors (1.65-fold; 95% CI: 1.27-2.13) compared to MSS (1.19-fold; 95% CI: 1.02-1.39). Dysregulation of these genes across these factors will broaden our understanding of 5-FU-based treatment in CRC. Furthermore, targeting dysregulated pathways could form the basis for improved precision therapies tailored to CRC subtypes. - Source: PubMed
Publication date: 2025/11/26
Islam Muhammad RafiqulJasmine FarzanaVasiljevs DaniilRaza MarufAlmazan ArmandoAhsan HabibulKibriya Muhammad G - Excessive lipolysis and inflammatory response are critically involved in the pathogenesis of ketosis in periparturient dairy cows. Evidence has been growing for participation of the growth hormone (GH) in the metabolic regulation of adipose tissue. However, the potential role of GH in promoting lipolysis and proinflammatory signaling activation in bovine adipocytes remains to be elucidated. The objective of this study was to investigate the regulatory effects of GH on the lipolysis and inflammatory response of bovine adipocytes. Subcutaneous adipose tissue and blood samples were collected from 10 healthy cows (blood BHB concentration <1.2 mM) and 10 cows with clinical ketosis (CK; blood BHB concentration >3.0 mM). For in vitro experiments, adipocytes were isolated from healthy Holstein cows. Differentiated adipocytes were used for (1) treatment with 0, 5, 10, or 15 ng/mL of GH for 8 h, or 15 ng/mL of GH for 0, 4, 8 or 12 h; (2) co-treatment with 15 ng/mL GH and 0.1 ng/mL tumor necrosis factor α (TNF-α); (3) pretreatment with 10 μM BAY 11-7082, a nuclear factor kappa B (NF-κB) inhibitor, and then treatment with 15 ng/mL GH. The CK cows displayed higher serum GH concentration. The protein abundance of phosphorylated lipolysis-limiting enzyme hormone sensitive lipase (HSL) was higher and mRNA abundance of lipid droplet coating proteins cell death-inducing DFFA-like effector c and perilipin 1 was lower in adipose tissue of CK cows versus healthy cows. The protein abundance of phosphorylated inhibitor of kappa B α (IκBα) and NF-κB, mRNA abundance of proinflammatory cytokines TNFA, NLR family pyrin domain containing 3 (NLRP3), IL-18 (IL18), caspase 1 (CASP1) and IL-1B (IL1B), and the activity of caspase 1 were greater in adipose tissue of CK cows, but protein abundance of IκBα was lower. In bovine adipocytes, GH induced lipolysis and inflammatory response, as evidenced by increased glycerol content in the supernatant and decreased cellular triglyceride content, as well as elevated phosphorylation levels of IκBα and NF-κB, decreased protein abundance of IκBα, upregulated mRNA abundance of TNFA, NLRP3, IL18, CASP1, and IL1B, and enhanced caspase 1 activity. Furthermore, TNF-α exacerbated GH-induced lipolysis and inflammation, whereas inhibition of NF-κB signaling pathway partially reverses these metabolic alterations of GH-treated adipocytes. These findings suggested that GH promote lipolysis in bovine adipocytes by activating inflammatory pathways. - Source: PubMed
Publication date: 2025/12/13
Gao XinxingYu HaoShi ZhaoxinSong ChenyangFang ZhiyuanGao WenwenLei LinSong YuxiangLi XinweiDu XiliangLiu Guowen - The causes of pelvic organ prolapse (POP) recurrence are sufficiently understood. Few studies have investigated the key genes of the recurrence of POP. In the present study, we screened the hub genes responsible for the recurrence of POP. The GSE28660 gene expression dataset contained microarray data of 4 recurrent POP and 4 primary POP uterosacral ligaments. We used the online gene expression omnibus microarray expression profiling dataset to identify differentially expressed genes. Further analyses of functional enrichment and protein-protein interaction networks (PPIs) were conducted, and key modules were identified. In the next step, we used the CIBERSORT algorithm to investigate differences in immune cell infiltration between recurrent and primary POP tissues. A total of 84 upregulated genes and 32 downregulated genes were identified. DNA microarray analysis of the human genome identified 116 genes associated with recurrence POP, and 2 hub genes, including cell death-inducing DFFA-like effector (CIDEA) and hemoglobin subunit delta (HBD), may contribute to the pathogenesis of recurrence POP, potentially providing diagnostic and therapeutic value. - Source: PubMed
Liu WenhuaZhang Yue - Intramuscular fat (IMF) content determines the quality of goat meat and is regulated by the comprehensive effect of the proliferation and adipogenesis of intramuscular preadipocytes. Our previous RNA-seq data revealed that cell death-inducing DNA fragmentation factor alpha (DFFA)-like effector (CIDE) A was upregulated during the development of intramuscular fat in the longissimus dorsi muscle tissue, implying an important role in lipid homeostasis. However, the mechanism by which , a member of the CIDE family, regulates intramuscular fat deposition in goat muscle is unknown, so we explored the function and underlying mechanism of in goat intramuscular preadipocytes. To address this, we altered in intramuscular preadipocytes and resolved the effect and mechanism of in adipogenesis through RT-PCR, Western blot, triglyceride and LD determinations, CCK-8, and RNA-seq. It was found that increased lipid droplets (LDs) and triglyceride contents and inhibited cell proliferation. Meanwhile, the lipid metabolism-related genes , , , , , , , , , , and were upregulated, while the lipolysis and β-oxidation genes , , and , as well as the proliferation marker gene , were all downregulated upon overexpression. Differentially expressed genes in dysregulation groups through RNA-seq were selected and were enriched in the apelin and focal adhesion signaling pathways. Specifically, the Western blot and rescue assays found that focal adhesion, but not apelin, was the key signaling pathway in regulating lipid deposition in goat intramuscular preadipocytes. In summary, this study reveals that promotes lipid deposition in intramuscular preadipocytes through the focal adhesion pathway and inhibits cell proliferation. This work clarifies the functional role and downstream signaling pathway of in intramuscular fat deposition and provides theoretical support for improving meat quality by targeting key phenotype-related genes. - Source: PubMed
Publication date: 2025/08/13
Shao PengLi QiLiao YuWang YongLin YaqiuXiang HuaDu ZhanyuZhang ChanghuiZhu JiangjiangHuang Lian